Glaucoma refers to a group of blinding neuropathies including primary open angle glaucoma (POAG), in which aqueous outflow is impeded resulting in increased intraocular pressure (IOP), and normal tension glaucoma (NTG), where pressure remains within a normal range but progressive loss of vision occurs. Worldwide, glaucoma affects over 60.5 million individuals, rendering it an enormous health problem. Elevated IOP is thought to damage the optic nerve resulting in progressive and irreversible blindness in glaucoma. Reduction in IOP remains the only proven therapy against glaucoma. Reduced aqueous humor (AH) outflow due to increased resistance to the former at the trabecular meshwork (TM), a tiny filter like region in the anterior eye, is attributed to elevated IOP. Prostaglandins (PGs), identified in the iris in 1955 as a smooth muscle stimulating substance, remain the only lipid class that is effective therapy for glaucoma as a topical application since 1997. The normal path of aqueous outflow is through the TM and is termed the conventional pathway. In the event of spikes of abnormal elevated pressure, an auxiliary pathway termed the uveoscleral pathway is often tapped transiently. Prostaglandin analogs increase aqueous outflow via the uveoscleral pathway. Except for pilocarpine, whose efficacy as a glaucoma drug is inferior to prostaglandins and with significant side effects, no known drug exists that increases the conventional outflow pathway. Thus, development of new therapeutics targeting the conventional pathway is warranted.